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(Circulation Research. 2004;94:1524.)
© 2004 American Heart Association, Inc.

Editorials

Breaking Down Cell-Cycle Barriers in the Adult Heart

Kelly M. Regula, Lorrie A. Kirshenbaum

From The Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre and the Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.

Correspondence to Dr Lorrie A. Kirshenbaum, Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Room 3016, 351 Taché Avenue, Winnipeg, Manitoba R2H 2A6, Canada. E-mail Lorrie@sbrc.ca

Key Words: regeneration • cell cycle • apoptosis • tumor-suppressor proteins • ventricular myocytes

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Over the past several years, there has been considerable interest in the ability of the adult myocardium to re-enter the cell cycle. From a historical perspective, the adult heart has generally been viewed as a nonproliferative organ with a limited and meager capacity for de novo myocyte regeneration and/or self-renewal after injury.^1,2 After birth, cardiac myocytes are believed to irreversibly exit from the cell cycle. As a result, growth of the postnatal heart occurs by hypertrophic rather than hyperplasic processes. The loss of functional cardiac myocytes through apoptotic/necrotic processes during ischemia or traumatic injury in the absence of de novo cell regeneration has been postulated to be an underlying cause of ventricular remodeling and diminished ventricular pump function. However, the recent discovery of cardiac progenitors within the myocardium itself,³ coupled with reports documenting the presence of adult myocytes synthesizing DNA in the nondiseased heart, has challenged the current dogma and has led to a re-evaluation of the true proliferative capacity of adult myocardium.⁴

Although it is generally accepted that adult ventricular myocytes do possess some capacity for DNA synthesis, there remains considerable debate as to whether differentiated postmitotic ventricular myocytes readily traverse the cell cycle, the frequency of synthetic events, and whether DNA synthesis coincides with a concomitant increase in cell number. Notwithstanding the acknowledged ability of adult myocytes to synthesize DNA, these limited events alone do not appear to be adequate to functionally restore diminished ventricular performance in patients with heart failure postmyocardial infarction. Given that myocyte number can . . . [Full Text of this Article]

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